Cholinergic modulation of synaptic function has been implicated in numerous aspects of learning, memory, and cognition, not only in hippocampus, but also in visual cortex. Intact Cholinergic innervation of visual cortex from Nucelus Basalis Magnocellularis (NBM) is required for visual memory processing and loss of Cholinergic input has been linked to symptoms in schizophrenia and Alzheimer's disease. Strengthening and weakening of synaptic function on short- and long-term time scales is believed to be a cellular correlate of learning and memory. In visual cortex, activation of muscarinic M1 receptors induces a long-term depression (mLTD) of glutamate transmission but the cellular mechanisms remain unknown. Preliminary data indicate that MAPK signaling is required and that mLTD expression is lost by lesion of NBM but is rescued in a time frame consistent with ingrowth of sympathetic fibers, a compensatory mechanism known to occur in hippocampus. The goal of this study is to determine the mechanisms by which acetylcholine modulates LTD in visual cortex, how forms of LTD are altered by loss of Cholinergic input, and whether there exists a compensatory mechanism, such as sympathetic sprouting, in visual cortex that maintains synaptic function. [unreadable] [unreadable] [unreadable]